Staphylococcus is a gram positive bacterium that occurs almost ubiquitously; most people carry staph organisms on their skin surfaces and nasal passages. Intact skin and mucosa are generally effective barriers to staph infections. Unfortunately, the converse is also true, with staph being the chief culprit in wound infections and abscesses. This article will focus on the two main groups of staphylococci and the infections they cause.
Staphylococcus aureus (henceforth abbreviated S. aureus) got its name from its ability to form gold colored colonies. S. aureus can also tolerate sodium chloride concentrations as high as 15%, or about five times the salt content of seawater. This bacterium is often the cause of wound infections as well as the formation of abscesses, or walled off pockets of infection. Unlike most other bacteria, S. aureus possesses an enzyme called coagulase, which causes human blood to clot, effectively shielding large numbers of these bacteria from destruction by white blood cells.
S. aureus is second only to streptococci as a leading cause of infective endocarditis and subacute bacterial endocarditis, abbreviated IE and SBE respectively. S. aureus is thought to be the culprit in 30% of cases of native valve endocarditis. Common symptoms of endocarditis include fever, a new onset heart murmur, splinter hemorrhages in the nail beds, joint and muscle pain, and anemia. Untreated IE is generally fatal within 6 weeks; even with treatment, the mortality rate is around 30%. In contrast, untreated SBE may take up to a year to be fatal, and if treated has an excellent prognosis.
In addition to abscesses and endocarditis, S. aureus also causes an array of other infections including food poisoning, Toxic Shock Syndrome, Staphylococcal scalded skin syndrome, and osteomyelitis (bone infection). Immune compromised people are also susceptible to pneumonia, meningitis, and other systemic infections caused by S. aureus.
Treatment of Staphylococcus aureus infections
Most S. aureus abscesses require surgical debridement and drainage. In addition to wound care, a course of broad spectrum antibiotics is warranted. First line agents include cephalosporins, especially cefazolin; piperacillin/tazobactam (Zosyn); and methicillin. Over the past several years, however, multiple drug resistant strains of S. aureus have emerged, in hospitals, collectively known as MRSA (which originally stood for methicillin resistant staph. aureus). The one reliable treatment for MRSA is a glycopeptide antibiotic called Vancomycin. Many physicians and microbiologists are convinced that, in the not too distant future, strains of Vancomycin resistant staphylococci (VRSA) will become a serious problem in hospitals across the United States.
Coagulase Negative Staphylococci
Clinicians sometimes refer to all other strains of staphylococci as coagulase negative staph, or CNS for short. CNS are a leading cause of nosocomial, or hospital acquired infections. S. saprophyticus mainly causes urinary tract infections, predominantly in patients with indwelling bladder catheters. These UTIs generally respond well to antibiotic therapy.
Another CNS, S. epidermidis can cause serious infections due to its tendency to colonize heart valves, especially prosthetic ones. A potentially fatal complication of S. epidermidis infection is prosthetic heart valve rupture. This form of CNS is also thought to cause up to 6% of native valve endocarditis infections as well.
Since most infections caused by CNS are hospital acquired, the general rule is empiric treatment with Vancomycin. If sensitivity cultures reveal the CNS to be susceptible to narrow spectrum antibiotics, these can be substituted for Vancomycin.
